| Project/Area Number |
15K19756
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Psychiatric science
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| Research Institution | Nara Medical University (2017)
National Institutes for Quantum and Radiological Science and Technology (2015-2016) |
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Principal Investigator |
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| Research Collaborator |
SHIMADA Hitoshi
SHINOTOH Hitoshi
HIRANO Shigeki
KUWABARA Satoshi
TAKAHATA Keisuke
MORIGUCHI Sho
NAGASHIMA Tomohisa
|
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2017: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | アルツハイマー病 / 行動心理症状 / タウ蛋白 / 前頭葉 / 眼窩前頭皮質 / 鉤状束 / アパシー / PET / アルツハイマー型認知症 / 認知症 / MRI |
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| Outline of Final Research Achievements |
Pathological phospholyrated tau accumulation is main neuropathology in Alzheimer's disease (AD). Progressive cognitive impairment in AD is known to be associated with the spread of tau accumulation, while the relationship between behavioral and psychological symptom (BPSD) and tau accumulation in AD is unclear. The present study examined the relationship between BPSD and tau accumulation with tau PET ligand 11C-PBB3. Our data found that tau accumulation in frontal cortex, especially orbitofrontal cortex (OFC), was significantly associated with apathy, frequently show in AD. Additionally, tau accumulation in OFC was attributable to the apathy directly and through the cortical thinning in OFC and consequent white matter disruption in uncinate fasciculus. These findings suggest that tau induced focal and network disruption in frontal cortex is considered to be of critical importance for apathy in AD.
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